The Contribution of the Intestinal Microbiota to the Celiac Disease Pathogenesis along with the Effectiveness of Probiotic Therapy

Abstract

The development of many human disorders, including celiac disease (CD), is thought to be influenced by the microbiota of the gastrointestinal tract and its metabolites, according to current research. This study's goal was to provide a concise summary of the information on the contribution of the intestinal microbiota to the CD pathogenesis, which was actively addressed while examining the reported pathogenesis of celiac disease (CD). We assumed that a change in gluten tolerance is formed under the influence of a number of different factors, including genetic predisposition and environmental factors. In related investigations, researchers have paid increasing attention to the study of disturbances in the composition of the intestinal microbiota and its functional activity in CD. A key finding of our review is that the intestinal microbiota has gluten-degrading properties, which, in turn, may have a protective effect on the development of CD. The intestinal microbiota contributes to maintaining the integrity of the intestinal barrier, preventing the formation of a "leaky" intestine. On the contrary, a change in the composition of the microbiota can act as a significant link in the pathogenesis of gluten intolerance and exacerbate the course of the disease. The possibility of modulating the composition of the microbiota by prescribing probiotic preparations is being considered. The effectiveness of the use of probiotics containing Lactobacillus and Bifidobacterium bacteria in experimental and clinical studies as a preventive and therapeutic agent has been documented.

Keywords: celiac disease; gluten; gluten enteropathy; gut microbiota; immune response; intestinal permeability; probiotics.

Figure 1

The intestinal mucosal–epithelial barrier in normal circumstances. It consists of pre-epithelial, epithelial and subepithelial levels. The pre-epithelial level is represented by a mucus layer. The epithelial level is represented by enterocytes, which are also closely connected by desmosomes. The subepithelial level includes lamina propria with immune cells.

Figure 2

The intestinal mucosal–epithelial barrier in celiac disease. Gluten undergoes decomposition to gliadin peptides, which bind with the type 3 chemokine receptor (CXCR3) and cause the release of zonulin. This increases the gaps between cells and penetration of gliadin into lamina propria. Gliadin peptides contribute to the activation of the innate immune response.